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Topics In Audiology > 1) Neural Plasticity > Flashcards

1) Neural Plasticity Flashcards

1
Q

Define neuroplasticity

A
  • Neuroplasticity, also known as neural plasticity or brain plasticity:
  • “Neuroplasticity is a process that involves adaptive structural and functional alterations to the brain in response to change”.
  • “Neuroplasticity refers to changes in the brain in response to experience.”
  • The ability for the brain to reorganize itself based on stimulation (changeable and flexible to exposure and changes in the environment
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2
Q

Define neuroplasticity in clinical terms

A

Clinically, it refers to brain changes after injury or intervention, such as:
̶- Hearing loss, tinnitus, or noise exposure (auditory disorders)
̶- Using hearing aids, cochlear implants, or aural rehabilitation programs (intervention)

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3
Q

These changes in neuroplasticity can be:

A

̶- Negative (detrimental): e.g.: Auditory deprivation, tinnitus, noise exposure
̶- Positive (beneficial): e.g.: Using auditory interventions to restore function

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4
Q

What 2 major mechanisms can neuroplasticity be broken down into?

A

1) structural neuroplasticity
2) functional neuroplasticity

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5
Q

Define structural neuroplasticity

A

Structural Neuroplasticity: Changes in the physical structure of the brain post-experience, E.g.:
- As a result of using CI post years of auditory deprivation).
- Brain damage and loss of auditory neural fibers post meningitis.
- Significant loss of AN fibers

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6
Q

How is structural neuroplasticity characterized (what are 3 more names for it)?

A

It is characterized by terms such as:
- Neuronal regeneration, neurogenesis, or synaptic plasticity.

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7
Q

Can you track structural neuroplasticity?

A

Yes, able to image the brain and track and monitor changes in the brain

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8
Q

Define functional neuroplasticity

A

Functional Neuroplasticity or Functional Reorganization (changes in function), e.g.:
- Multilingualism
- Learning different skills
- Brain laterality in children leading to right/left-handedness, eyedness, or footedness.
- Learning to drive, functionally your brain changes, but no structural change

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9
Q

How is functional neuroplasticity different than structural neuroplasticity?

A
  • Changes in function, but not seeing any changes in brain structure
  • Clinically, not expecting any changes in brain structure
  • See significant change in function with fMRI (but structure MRI, there is no difference)
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10
Q

Neuroplasticity following injury is thought to occur in ____ phases or epochs

A

Three

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11
Q

What are the 3 phases of neuroplasticity that occur after injury?

A

1) First 48 hours
2) After two weeks
3) Weeks to months afterward

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12
Q

What happens in the first 48 hours after injury?

A
  • Consequent to damage, the brain attempts to use secondary neuronal networks to maintain
    function.
  • The auditory part of the brain has experienced significant damage and looking for other ways to process
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13
Q

What happens after 2 weeks after injury?

A

̶- The occurrence of synaptic plasticity and new connections.
̶- Recruitment of support cells (support cells replace the lost nerves; change the function).
̶- Shift of cortical pathways from inhibitory to excitatory.

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14
Q

What happens weeks to months after injury?

A

The brain continues to remodel itself via axonal sprouting and further reorganization around the damage.

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15
Q

What are two neuroplasticity mechanisms?

A

1) Neural Regeneration/Collateral Sprouting
2) Synaptic Plasticity

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16
Q

Define Neural Regeneration/Collateral Sprouting

A

The development of new neurons and connections after damage

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17
Q

What three things does Neural Regeneration/Collateral Sprouting depend on?

A
  • Age of the person
  • If the damage is peripheral or central
  • Size of damage
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18
Q

Define synaptic plasticity

A
  • Refers to changes in the strength of connections between neurons based on experiences.
  • Can be positive or negative
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19
Q

What are factors that positively influence synaptic plasticity?

A

Exercise, environment, repetition, motivation, neuromodulators (like dopamine), and supplements/medications.

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20
Q

What are factors that negatively influence synaptic plasticity?

A

Aging and neurodegenerative diseases.

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21
Q

What are the 3 types of plasticity in the auditory system?

A

1) Adaptive Plasticity
2) Experience-dependent Plasticity
3) Cross-Modal (CM) Plasticity

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22
Q

What is another name for adaptive plasticity?

A

Stimulus-specific Adaptation

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23
Q

Define adaptive plasticity/stimulus-specific adaptation

A

̶- Stimulus-specific adaptation (SA) refers to reduced neuronal response due to repeated exposure to a stimulus, and it does not generalize to other stimuli.
- Changes based on the inputs the brain is getting
- You get used to a certain exposure
- Very common with tinnitus

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24
Q

What 3 places is SA observed?

A

SA is observed in the auditory cortex (AC), midbrain, and thalamus.

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25
Q

How is SA often studied?

A

SA is often studied using an “oddball” paradigm in:
̶- Mismatch Negativity
̶- P3

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26
Q

What is the oddball paradigm?

A
  • Where rare signals (deviant signals) are presented amid common signals (standards). The adaptation to the standard stimulus while maintaining a robust response to the deviant signal suggests a role for SA in detecting novelty or deviance.
  • The brain’s response to the deviant signal will be different
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27
Q

What is an example of adaptive plasticity?

A

Change in Cortical Tonotopy after Partial
Hearing Loss

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28
Q

Explain how changes in cortical tonotopy after PHL occurs with adaptive plasticity

A
  • Following PHL, Cortical neurons in the damaged area develop new characteristic frequencies (CFs) similar to frequencies represented at the edge(s) of the cochlear lesion.
  • Then, this brain region is wholly or partly occupied by the expanded representation of the lesion-edge frequency or frequencies.
  • This change in cortical tonotopy occurs some weeks or months after the cochlear insult
  • All parts of the damaged area (gray area) start responding to the same frequency (the edge frequency)
  • Over representation of certain frequencies
  • This is tinnitus or over-representation of sound
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29
Q

What three ways does tinnitus occur in those with PHL?

A

1) The expanded representation of lesion-edge frequencies
2) Increased spontaneous neural firing rates at edge frequencies
3) Hyperacusis and tinnitus

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30
Q

Tinnitus distress/emotional reactions to tinnitus undoubtedly depend on (2):

A
  • The connections of the AC with higher cognitive and affective brain areas
  • As an indication of Maladaptive Plasticity
31
Q

Tinnitus perception is relative to the ____

A

Auditory system

32
Q

Are the symptoms associated with tinnitus due to a system other than the auditory system?

A
  • Yes, symptoms associated to tinnitus are due to a different system (some people with tinnitus cannot cope)
  • Maladaptive brain plasticity (the auditory cortex begins making connects that are not correct)
33
Q

Chronic, bothersome tinnitus drives large-scale ____

A

Maladaptive plasticity

34
Q

Correlated with behavioral changes in tinnitus, such as (4):

A

̶- Frustration
̶- Inability to relax
̶- Difficulty in concentration
̶- Impaired executive control of attention and working memory

35
Q

Several brain networks are involved in tinnitus ____, ____, and ____.

A

perception, persistence, annoyance

36
Q

Explain maladaptive connections

A
  • When someone feels distressed from tinnitus, it is because of making bad connections within the brain (activating large neural networks associated with emotions)
  • Hippocampus will make a memory of the tinnitus sound (which is not good)
  • It is difficult to break these connections of maladaptive plasticity
  • These connections lead to very bothersome tinnitus and these patients have a difficult time coping
37
Q

What are the 4 negative maladaptive plasticity mechanisms that can be formed due to tinnitus?

A

1) Perception/awareness network
2) The salience network (SN): contribute to processing novel stimuli; tinnitus.
3) Tinnitus annoyance/distress network
4) Memory mechanisms: persistence of the phantom perception of sound

38
Q

Define experience-dependent plasticity

A
  • A broad term, referring to structural or functional plasticity due to exposure or environmental experiences.
  • Reorganization of the brain based on experience and exposure
  • Occurs in the brain everyday
  • Structural differences can change with long term exposure
39
Q

What are some examples of experience-dependent plasticity?

A

Brain structural/functional plasticity in:
̶- Musicians
̶- Bilinguals
̶- Athletes / Professional players
̶- Auditory training: detection, discrimination, or identification tasks.
̶ - E.g.: The expansion/enlargement of auditory cortical tonotopy in trained frequencies in animals

40
Q

How does experience-dependent plasticity in the brainstem in musicians work?

A
  • Neuroplasticity isn’t limited to the auditory cortex (it is happening in the lower brainstem)
  • We can track changes in neuroplasticity through CABR
41
Q

What is FFR?

A
  • Frequency following response
  • FFR is a scalp-recorded periodic auditory evoked potential (AEP) that closely resembles the evoking stimulus.
  • The FFR reflects sustained phase-locked activity in a population of neural units within the brainstem.
  • The brain responses is mimicking exactly what is happening in the stimulus (the brain is phase locking to the details of the presentation) = FFR
  • The brain is phase locked in functional and structural imaging
42
Q

FRR is recorded by ____

A

Complex auditory stimuli

43
Q

What 2 types of complex auditory stimuli can be used to record FFR?

A

‒ Music tones, e.g.: a piano or guitar tone
‒ Speech syllables, e.g.: /da/, /ba/, /ga/, pa/

44
Q

What is CABR?

A
  • Complex ABR (the complexity of the stimulus used for the ABR)
  • Uses music or speech (a click is used in typical ABR)
  • FFR is part of CABR
45
Q

Define cross-modal (CM) plasticity

A

Cross-modal plasticity is an adaptive feature of the brain, whereby the loss of one sensory modality (auditory) induces cortical reorganization leading to enhanced sensory performance in remaining modalities (visual and tactile).

46
Q

What 2 instances is CM plasticity observed?

A

1) It is observed in children with late hearing loss identification and intervention (hearing aids or cochlear implants).
2) In children with congenital or prelingual deafness (C/PD)

47
Q

CM plasticity expectations for early implantation:

A
  • Improved spontaneous neural activity in auditory and spoken-language brain areas.
  • Rapid normalization of the P1 wave latency correlating with speech perception outcomes.
48
Q

CM plasticity expectations for late implantation:

A
  • High spontaneous neural activity before CIs. It is evidence of CM recruitment of the AC by vision and touch (it has already been taken over by other systems; it is very hard to get the auditory system back to what it used to be).
  • Abnormal/absent P1/AEPs even after years of implant use, indicating a sensitive period for cochlear implantation.
49
Q

Explain CM plasticity in CI users

A
  • The P1 cortical auditory evoked potential (CAEP) serves as a biomarker for AC maturation and CI outcomes.
  • There is a sensitive period for optimal CI outcomes.
  • It is recommended to receive CIs before 3.5 years
50
Q

What happens if you get a CI before 3.5 years?

A

CI before 3.5 years often results in normal P1 responses over time.

51
Q

What happens if you get a CI after 7 years?

A
  • CI after 7 years leads to abnormal/absent P1 responses, suggesting a crucial
  • Window for intervention
52
Q

What happens if you get a CI between 3.5 and 7 years?

A

P1 may or may not reach the normal limits.

53
Q

Studies indicate correlations between CM recruitment of the AC with visual/tactile stimuli and ____

A

Poor CI outcomes.

54
Q

Case Report 1: Tracking HA Performance with P1

A
  • The case study involves a child with auditory neuropathy spectrum disorder (ANSD)
  • There were initial concerns about the effectiveness of hearing aids (HAS).
  • However, behavioral testing and improved P1 latency post-HA fitting were suggestive of successful use of HAs and normal AC development.
  • Note: The case supports the idea that some children with ANSD may benefit from early intervention with HAs.
  • After receiving HAs, P1 normalized
55
Q

What are the 2 types of AN?

A
  • Post-synaptic AN: involvement of the AN and brainstem
  • Pre-synaptic AN: IHCs and ANFs = this people do better with intervention (HA and CI); the brain itself isn’t impacted, so as long as we can get the information to the auditory nerve/brain, these people can do well
56
Q

Will everyone with HAs improve P1 latency?

A
  • Depends on lesion site (IHC, AN fibers, or low brainstem)
  • Because of dependence on lesion site, treatment can be difficult
57
Q

Case Report 2: Tracking CI Performance with P1

A
  • Case 2 was born prematurely with ANSD.
  • Despite early fitting hearing aids, there were:
    • Language delays in SLP assessments
    • Absent P1 responses in 2 assessments.
  • Post CI: Gradual improvement of P1 reaching to normal limits by 2.18 years.
  • Overall, ANSD resulting from cochlear or synaptic lesions are more likely to benefit from CIs than post-synaptic lesions.
  • Worse results as we go up in lesion site (involvement of AN and HCs)
58
Q

Case Report 3: Tracking CI Performance with P1

A

A case with:
̶- No birth complications.
̶- Bilateral profound SNHL.
̶- Inconsistent results with bilateral HAs.
̶- Received a CI at 1.64 years.
̶- Diminished initial positive outcomes over time, correlating with poor behavioral outcomes.

  • The case underscores the complexity of ANSD, emphasizing the need for individualized/customized approaches in ANSD management
  • response at a lower age, then after that there is no response
  • this is linked to involvement of progressive AN (involved higher parts of the auditory system including the higher brainstem)
  • this is common in genetic AN- started pre-synaptic and progressed too post-synaptic
  • those with genetic AN are not good candidates for CIs
59
Q

***Case Report 4: Tracking CI Performance with fMRI

A

CM Plasticity in Good vs. Average CI Performers

fMRI with visual stimuli (A) and tactile stimuli (B) in:
̶- A child with normal hearing
̶- A child as a good CI user
̶- A child as an average CI user

Figure A: fMRI with visual stimuli :
̶- Children 1 and 2: visual cortex (VC) recruitment by visual stimuli
̶- Child 3: both AC and VC recruitment by visual stimuli

Figure B: fMRI with tactile stimuli
̶- Children 1 and 2: Parietal cortex (PC) recruitment by tactile stimuli
̶- Child 3: both AC and PC recruitment by tactile stimuli

60
Q

What is case report 4 showing?

A

This is showing cross-modal plasticity (can use imaging to track this)

61
Q

What are the conclusions for CM plasticity in children with CIs?

A

Expected P1 Latency and Speech Perception Outcomes Based on Age of Implantation:
̶- Early implantation (<3.5 years) often leads to P1 latencies within normal limits + optimal CI outcomes
̶- Late implantation (>6.5–7 years) results in abnormal/absent P1 responses even after years of use (high likelihood of CM plasticity)
̶- CIs between 3.5 and 7 years show variable outcomes.
- This is a confirmation for: A sensitive period for AC maturation.
- Recording visual or tactile evoked responses from the AC in a marker of CM plasticity
- Age of implantation is very important

62
Q

Case Report 5: CM Plasticity in Unilateral Deafness

A

̶- A child late-identified with moderate SNHL in the right ear at age 5 and normal hearing in the left ear.
̶- Progression to profound SNHL at age 9.
̶- CI for the RE at age 10.

63
Q

Case Report 5 - Before CI:

A

̶- CM recruitment of AC with vision (A) and touch (B).
̶- (C) Activation of AC and frontal and prefrontal areas by auditory.
- The frontal cortex activation may indicate “effortful listening”, and the need for the recruitment of additional resources to process auditory information.

64
Q

Case Report 5 - After CI:

A

̶- Partial reversal of the recruitment of AC with vision.
̶- Total reversal of the recruitment of AC with touch.
̶- A more typical pattern of auditory activation.

65
Q

Case Report 6: CM Plasticity in Adults with Mild to Moderate Hearing Loss

A

An adult male with bilateral mild-to-moderate hearing loss.
- (A) CM recruitment of AC by vision: Activation of both AC and VC by visual stimuli.
- (B) Total reversal of CM recruitment of AC by vision within 30 days of HA use.
- (C) Improved behavioral performance after 30 days of HA use:
- Improved speech-in-noise scores
- Decreased dependence on visual cues for speech perception.
- Increased global cognitive function.

66
Q

Case Report 7: CM Plasticity in Long-term Hearing Aid Users

A
  • Brain reorganization in excellent and poor long-term HA users.
  • Both are adults with mild-to-moderate hearing loss and at least 18 months of HA experience.
  • (A) Excellent Performer:
    • Expected activation of the VC by visual stimuli (no evidence of CM recruitment)
    • Excellent speech in noise performance.
      (B) Poor Performer:
    • CM recruitment of the AC with vision
    • Poor speech in noise outcomes.
67
Q

CM plasticity is detrimental when:

A

̶- The goal of the auditory rehabilitation program is set to learn spoken language through the auditory system alone (i.e., uni-sensory communication mode or aural rehabilitation approach).
̶- It applies to children who receive CIs during sensitive periods of spoken language development.

68
Q

CM plasticity could be beneficial when:

A

̶- The rehabilitation goal is set to enhance communication skills using a multisensory approach (i.e., total communication mode)
- After injury

69
Q

It is very difficult to regrow connections after ____

A

CM plasticity

70
Q

CM plasticity is common in ____.

A

Auditory disorders

71
Q

CM plasticity may or may not be ____ by HAs or CIs.

A

Partially/totally reversed

72
Q

____ and ____ can serve as biomarkers of CM plasticity and HA/CI outcomes.

A

P1, neuroimaging

73
Q

These three tools may help clinicians:

A

1) Determine when a patient should receive intervention.
̶2) Determine what kind of intervention or rehabilitation would be ideal.
̶3) Monitor how well a chosen intervention or rehabilitation method is working

Topics In Audiology (6 decks)

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